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PMID |
Sentence |
1 |
16038020
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Cytokine interleukin-12 (IL-12) is one of the key factors in the differentiation of naïve CD4(+) T cells into Th1 cells.
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2 |
16038020
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In this study we used 2-DE and MS to find and identify IL-12 regulated proteins in human CD4(+) T cells.
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3 |
16038020
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Among the upregulated proteins there are a multifunctional cytokine macrophage migration inhibitory factor and a known IL-12 target gene Programmed cell death 4.
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4 |
16038020
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Downregulated proteins include p21-activated kinase 2 and its upstream GTPase Cdc42.
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5 |
16038020
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Compared to previous reports our analysis provides a new view on the IL-12 induced changes on CD4(+) T cells underscoring the importance of creating and combining the data generated at various levels to build a comprehensive view of a given biological process of the cell.
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6 |
18549351
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Knockdown of Pdcd4 results in induction of proprotein convertase 1/3 and potent secretion of chromogranin A and secretogranin II in a neuroendocrine cell line.
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7 |
21730150
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Here we describe a unique regulatory pathway of β cell death that comprises microRNA-21, its target tumor suppressor PDCD4, and its upstream transcriptional activator nuclear factor-κB (NF-κB).
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8 |
21730150
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In pancreatic β cells, c-Rel and p65 of the NF-κB family activated the mir21 gene promoter and increased miR-21 RNA levels; miR-21 in turn decreased the level of PDCD4, which is able to induce cell death through the Bax family of apoptotic proteins.
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9 |
21730150
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Here we describe a unique regulatory pathway of β cell death that comprises microRNA-21, its target tumor suppressor PDCD4, and its upstream transcriptional activator nuclear factor-κB (NF-κB).
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10 |
21730150
|
In pancreatic β cells, c-Rel and p65 of the NF-κB family activated the mir21 gene promoter and increased miR-21 RNA levels; miR-21 in turn decreased the level of PDCD4, which is able to induce cell death through the Bax family of apoptotic proteins.
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11 |
22158625
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High glucose stimulated mTORC1 to promote key events in the initiation and elongation phases of mRNA translation: binding of eIF4A to eIF4G, reduction in PDCD4 expression and inhibition of its binding to eIF4A, eEF2 kinase phosphorylation, and dephosphorylation of eEF2; these events were inhibited by NaHS.
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12 |
22158625
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NaHS induction of AMPK phosphorylation was inhibited by siRNA for calmodulin kinase kinase β, but not LKB1, upstream kinases for AMPK; STO-609, a calmodulin kinase kinase β inhibitor, had the same effect.
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13 |
22655170
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Overexpression of miR-21 in insulin-secreting MIN6 cells downregulated endogenous expression of the tumor suppressor Pdcd4 and of Pclo, a Ca(2+) sensor protein involved in insulin secretion.
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14 |
23990362
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Programmed cell death-4 deficiency prevents diet-induced obesity, adipose tissue inflammation, and insulin resistance.
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15 |
23990362
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This study aims to investigate the effects of PDCD4 on obesity, inflammation, and insulin resistance.
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16 |
23990362
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Surprisingly, high-fat diet (HFD)-fed PDCD4-deficient (PDCD4(-/-)) mice exhibited an absolutely lean phenotype together with improved insulin sensitivity.
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17 |
23990362
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Importantly, PDCD4 appeared to disturb lipid metabolism via inhibiting the expression of liver X receptor (LXR)-α, a master modulator of lipid homeostasis, which was elevated in HFD-fed PDCD4(-/-) mice accompanied by upregulation of its target genes and relieved endoplasmic reticulum stress in WAT.
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18 |
23990362
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These data demonstrate that PDCD4 deficiency protects mice against diet-induced obesity, WAT inflammation, and insulin resistance through restoring the expression of LXR-α, thereby proposing PDCD4 as a potential target for treating obesity-associated diseases.
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19 |
23990362
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Programmed cell death-4 deficiency prevents diet-induced obesity, adipose tissue inflammation, and insulin resistance.
|
20 |
23990362
|
This study aims to investigate the effects of PDCD4 on obesity, inflammation, and insulin resistance.
|
21 |
23990362
|
Surprisingly, high-fat diet (HFD)-fed PDCD4-deficient (PDCD4(-/-)) mice exhibited an absolutely lean phenotype together with improved insulin sensitivity.
|
22 |
23990362
|
Importantly, PDCD4 appeared to disturb lipid metabolism via inhibiting the expression of liver X receptor (LXR)-α, a master modulator of lipid homeostasis, which was elevated in HFD-fed PDCD4(-/-) mice accompanied by upregulation of its target genes and relieved endoplasmic reticulum stress in WAT.
|
23 |
23990362
|
These data demonstrate that PDCD4 deficiency protects mice against diet-induced obesity, WAT inflammation, and insulin resistance through restoring the expression of LXR-α, thereby proposing PDCD4 as a potential target for treating obesity-associated diseases.
|
24 |
23990362
|
Programmed cell death-4 deficiency prevents diet-induced obesity, adipose tissue inflammation, and insulin resistance.
|
25 |
23990362
|
This study aims to investigate the effects of PDCD4 on obesity, inflammation, and insulin resistance.
|
26 |
23990362
|
Surprisingly, high-fat diet (HFD)-fed PDCD4-deficient (PDCD4(-/-)) mice exhibited an absolutely lean phenotype together with improved insulin sensitivity.
|
27 |
23990362
|
Importantly, PDCD4 appeared to disturb lipid metabolism via inhibiting the expression of liver X receptor (LXR)-α, a master modulator of lipid homeostasis, which was elevated in HFD-fed PDCD4(-/-) mice accompanied by upregulation of its target genes and relieved endoplasmic reticulum stress in WAT.
|
28 |
23990362
|
These data demonstrate that PDCD4 deficiency protects mice against diet-induced obesity, WAT inflammation, and insulin resistance through restoring the expression of LXR-α, thereby proposing PDCD4 as a potential target for treating obesity-associated diseases.
|
29 |
23990362
|
Programmed cell death-4 deficiency prevents diet-induced obesity, adipose tissue inflammation, and insulin resistance.
|
30 |
23990362
|
This study aims to investigate the effects of PDCD4 on obesity, inflammation, and insulin resistance.
|
31 |
23990362
|
Surprisingly, high-fat diet (HFD)-fed PDCD4-deficient (PDCD4(-/-)) mice exhibited an absolutely lean phenotype together with improved insulin sensitivity.
|
32 |
23990362
|
Importantly, PDCD4 appeared to disturb lipid metabolism via inhibiting the expression of liver X receptor (LXR)-α, a master modulator of lipid homeostasis, which was elevated in HFD-fed PDCD4(-/-) mice accompanied by upregulation of its target genes and relieved endoplasmic reticulum stress in WAT.
|
33 |
23990362
|
These data demonstrate that PDCD4 deficiency protects mice against diet-induced obesity, WAT inflammation, and insulin resistance through restoring the expression of LXR-α, thereby proposing PDCD4 as a potential target for treating obesity-associated diseases.
|
34 |
23990362
|
Programmed cell death-4 deficiency prevents diet-induced obesity, adipose tissue inflammation, and insulin resistance.
|
35 |
23990362
|
This study aims to investigate the effects of PDCD4 on obesity, inflammation, and insulin resistance.
|
36 |
23990362
|
Surprisingly, high-fat diet (HFD)-fed PDCD4-deficient (PDCD4(-/-)) mice exhibited an absolutely lean phenotype together with improved insulin sensitivity.
|
37 |
23990362
|
Importantly, PDCD4 appeared to disturb lipid metabolism via inhibiting the expression of liver X receptor (LXR)-α, a master modulator of lipid homeostasis, which was elevated in HFD-fed PDCD4(-/-) mice accompanied by upregulation of its target genes and relieved endoplasmic reticulum stress in WAT.
|
38 |
23990362
|
These data demonstrate that PDCD4 deficiency protects mice against diet-induced obesity, WAT inflammation, and insulin resistance through restoring the expression of LXR-α, thereby proposing PDCD4 as a potential target for treating obesity-associated diseases.
|